Aim: ATF3, a member of the ATF/CREB family of transcription factors, has been found to be selectively induced by calcineurin/NFAT inhibition and to enhance keratinocyte tumor formation, although the precise role of ATF3 in human skin cancer and possible mechanisms remain unknown. Methods: In this study, clinical analysis of 30 skin cancer patients and 30 normal donors revealed that ATF3 was accumulated in skin cancer tissues. Functional assays demonstrated that ATF3 significantly promoted skin cancer cell proliferation. Results: Mechanically, ATF3 activated Stat3 phosphorylation in skin cancer cell through regulation of p53 expression. Moreover, the promotion effect of ATF3 on skin cancer cell proliferation was dependent on the p53-Stat3 signaling cascade. Conclusion: Together, the results indicate that ATF3 might promote skin cancer cell proliferation and enhance skin keratinocyte tumor development through inhibiting p53 expression and then activating Stat3 phosphorylation.
A 20-year-old female patient presented with erythematous plaques on the nose which were progressively spreading to the trunk and the extremities, sometimes with erosions and scars. The patient was misdiagnosed as having seborrhoeic dermatitis and subacute cutaneous lupus erythematosus. The histopathological biopsy revealed mycotic infectious granuloma. Samples taken from skin lesions and other locations grew Trichosporon asahii in cultures. The identification was confirmed by molecular biological methods. The patient was treated successfully with liposomal amphotericin B in combination with fluconazole orally.
Spinal cord injury (SCI) is a catastrophic condition with high morbidity and mortality that still lacks effective therapeutic strategies. It is well known that the most important stage in SCI pathogenesis is secondary injury, and among the involved mechanisms, the inflammatory cascade is the main contributor and directly influences neurological function recovery. In recent years, increasing evidence has shown that mesenchymal stem cells (MSCs) transplantation is a promising immunomodulatory strategy. Transplanted MSCs can regulate macrophage-, astrocyte-, and T lymphocyte-mediated neuroinflammation and help create a microenvironment that facilitates tissue repair and regeneration. This review focuses on the effects of different types of immune cells and MSCs, specifically the immunoregulatory capacity of MSCs in SCI and repair. We will also discuss how to exploit MSCs transplantation to regulate immune cells and develop novel therapeutic strategies for SCI.
T richosporon species can cause biofilm-associated infections related to indwelling medical devices, especially intravenous catheters, and unacceptable mortality rates have been reported despite the administration of antifungal treatments (1). Trichosporon asahii can form biofilms with structured microbial communities in vitro, embedded within an extracellular matrix, with significantly increased resistance to antifungal compounds (2, 3), which might ultimately lead to clinical treatment failure. Antifungal combination may be an alternative therapy strategy for biofilm-related fungal infections (4). The synergistic effects of antifungal combinations against other fungal biofilms have been detected in vitro, such as amphotericin B-posaconazole for Candida albicans (5) and amphotericin B-caspofungin or voriconazole-caspofungin for Aspergillus spp. (6). The synergistic effects of antifungal combinations of voriconazole, amphotericin B, and caspofungin against planktonic T. asahii have been found in vitro (7). We evaluated the in vitro activity of the combinations of voriconazole-amphotericin B, voriconazole-caspofungin, and amphotericin B-caspofungin against 16 clinical isolates of T. asahii in biofilm and planktonic forms by a broth microdilution checkerboard method (5). Trichosporon biofilms were prepared according to the 96-well plate-based method (8). The effect of antifungal agents was determined by the 2,3-bis(2-methoxy-4-nitro-5-[(sulfenylamino)carbonyl]-2H-tetrazolium hydroxide (XTT)-based colorimetric assay for both biofilms and planktonic cells (5,8). The MIC and sessile MIC (SMIC) were determined as the lowest antifungal concentration (alone or in combination) that caused a 50% reduction in optical density for both biofilms and planktonic cells compared with the growth control (5, 6). The interaction was defined on the basis of the fractional inhibitory concentration indexes (FICIs) as follows: Յ0.5, synergy; Ͼ0.5 to 4, indifference; and Ͼ4.0, antagonism.Under planktonic conditions, the amphotericin B-caspofungin combination showed the highest percentage of synergistic effects (81.25%; FICI, 0.125 to 0.5) ( Table 1), as indicated by a previous in vitro study (7). Under biofilm conditions, the voriconazole-amphotericin B combination showed the highest percentage of synergistic effects (87.5%; FICI, 0.078 to 0.313), and the SMIC 90 /SMIC ranges for these two drugs obviously decreased from Ͼ1,024/512 to Ͼ1,024 g/ml to 64/4 to 128 g/ml for voriconazole and from 1,024/32 to 1,024 g/ml to 32/4 to 128 g/ml for amphotericin B, respectively. The combinations of amphotericin B-caspofungin (93.75%) and voriconazole-caspofungin (81.25%) mainly yielded indifferent interactions, and no antagonistic interaction was observed in any of the combinations of either the biofilms or the planktonic forms of T. asahii isolates (Table 1).Trichosporon now ranks as the second most common pathogen causing fungemia in patients with hematological malignant disease, mainly catheter-related bloodstream infections (CR-BSIs) (1, 9). For ...
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